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Role of Methionine Adenosyltransferase Genes in Hepatocarcinogenesis
Division of Gastroenterology and Liver Diseases, USC Research Center for Liver Diseases, Southern California Research Center for Alcoholic Liver and Pancreatic Diseases & Cirrhosis, Keck School of Medicine USC, Los Angeles, California 90033, USA
CIC bioGUNE, Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas (Ciberehd), Technology, Park of Bizkaia, 48160 Derio, Bizkaia, Spain
* Author to whom correspondence should be addressed.
Received: 16 December 2010; in revised form: 27 January 2011 / Accepted: 30 January 2011 / Published: 24 March 2011
Abstract: Hepatocellular carcinoma (HCC) is the most common primary malignant tumor of the liver. Detection of HCC can be difficult, as most of the patients who develop this tumor have no symptoms other than those related to their longstanding liver disease. There is an urgent need to understand the molecular mechanisms that are responsible for the development of this disease so that appropriate therapies can be designed. Methionine adenosyltransferase (MAT) is an essential enzyme required for the biosynthesis of S-adenosylmethionine (AdoMet), an important methyl donor in the cell. Alterations in the expression of MAT genes and a decline in AdoMet biosynthesis are known to be associated with liver injury, cirrhosis and HCC. This review focuses on the role of MAT genes in HCC development and the scope for therapeutic strategies using these genes.
Keywords: methionine adenosyltransferase (MAT); hepatocellular carcinoma (HCC); S-adenosylmethionine (AdoMet)
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Cite This Article
MDPI and ACS Style
Ramani, K.; Mato, J.M.; Lu, S.C. Role of Methionine Adenosyltransferase Genes in Hepatocarcinogenesis. Cancers 2011, 3, 1480-1497.
Ramani K, Mato JM, Lu SC. Role of Methionine Adenosyltransferase Genes in Hepatocarcinogenesis. Cancers. 2011; 3(2):1480-1497.
Ramani, Komal; Mato, José M.; Lu, Shelly C. 2011. "Role of Methionine Adenosyltransferase Genes in Hepatocarcinogenesis." Cancers 3, no. 2: 1480-1497.